Figure 4.
Inhibition of autophagy reverses the effects of BA on pyroptosis after SCI. (A) Immunofluorescence staining for p62 and NeuN co-localization at the spinal cord lesion after SCI (scale bar = 25 µm). (B) The quantitative mean optical density of the p62 in motor neurons of spinal cord lesion in each group. (C) Immunofluorescence staining for LC3II and NeuN co-localization at the spinal cord lesion after SCI (scale bar = 25 µm). (D) The quantitative mean number of the LC3II positive neurons in motor neurons of spinal cord lesion in each group. (E) Western blotting for the p62, LC3II, Beclin1, Vps34, and CTSD expression levels in the BA and BA+3MA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the p62, LC3II, Beclin1, Vps34, and CTSD expression levels were quantified and analyzed in each group. (G) Immunofluorescence staining for Caspase-1 and NeuN co-localization in the spinal cords of the BA and BA+3MA groups (scale bar = 25 µm) (H) The quantitative mean optical density of the Caspase-1 in motor neurons of spinal cord lesion. (I) Immunofluorescence staining for GSDMD and NeuN co-localization in the spinal cords of the BA and BA+3MA groups (scale bar = 25 µm) (J) The quantitative mean optical density of the GSDMD in motor neurons of spinal cord lesion. (K) Western blotting for the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels in the BA and BA+3MA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (L) The optical density values of the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. *p< 0.05 and **p< 0.01, vs. BA group.
